Rituximab-induced lung injury is a rare but serious side effect of this agent. We describe the valuable role played by 18-F fluorodeoxyglucose positron emission tomography-computed tomography (FDG PET-CT) in the diagnosis and follow-up of this condition in a patient with non-Hodgkin’s lymphoma (NHL) receiving rituximab (Fig. 1). Abnormal uptake of FDG in lungs of patients receiving this drug should be carefully evaluated to diagnose this potentially fatal side effect.
Fig. 1.
A 53-year-old woman underwent 18-F fluorodeoxyglucose positron emission tomography-computed tomography (FDG PET/CT) for staging of non-Hodgkin’s lymphoma. The scan (Fig. 1a) revealed increased FDG uptake in multiple lymph nodes (black arrows), an enlarged spleen (blue arrow) and bone marrow (red arrow), suggesting stage IV disease. Post two cycles of chemotherapy with the rituximab-CHOP protocol, PET-CT was performed for response assessment. The scan (Fig. 1b) showed complete metabolic response in previously seen lesions. However, new diffuse, intense FDG uptake (SUVmax = 6.5) was noted in bilateral lung fields, which on CT demonstrated a diffuse ground-glass appearance. The patient had no history of pulmonary disease and complained of a persistent dry cough after the end of the second cycle of chemotherapy. Considering the metabolic response in previously seen lesions, we reported the new lung findings as suspicious for drug-induced pulmonary toxicity, possibly because of rituximab. A short course of steroids was prescribed, and rituximab was omitted from further chemotherapy. After discontinuation of rituximab, the patient reported an improvement in symptoms. On completion of chemotherapy, PET/CT (Fig. 1c) showed the disappearance of diffuse FDG uptake in the lungs, and also the CT findings reverted back to normal. We concluded that the interim PET/CT scan findings showed rituximab-induced drug toxicity. Rituximab-induced lung injury is a rare but potentially fatal complication that occurs in around 0.03 % of patients [1]. Treatment with rituximab results in the activation of complement, B-lymphocyte cytolysis, and the release of tumor necrosis factor α [2]. Cytokine release is proposed as the mechanism for the development of interstitial pneumonitis [3]. Though rare, this possibility should be considered in patients who develop respiratory symptoms or new imaging findings while receiving this agent
Conflict of Interest
We declare that we have no conflict of interest.
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